Puccinia triticina effector Pt_20 ₆₃₆ triggers PCD in TcLr16 wheat promoted by TaLhcb4 .1 via the ROS pathway

SUMMARY As an obligate biotrophic pathogen, Puccinia triticina ( Pt ) subverts wheat immunity via effector delivery. However, the molecular mechanisms underlying Pt effector‐mediated wheat susceptibility remain largely unexplored. In this study, an effector Pt_20 that is induced expression at the early stage of Pt infection to wheat was identified. Interestingly, the Pt_20 gene exhibits two distinct transcriptional isoforms ( Pt_20 636 , Pt_20 807 ) among Pt races and both are localized in the nucleus, cytoplasm, and plasma membrane. Pt_20 636 was able to suppress BAX‐mediated cell death in Nicotiana benthamiana, but Pt_20 807 was not. Importantly, Pt_20 636 triggers Lr16 ‐dependent cell death, though Pt_20 807 does not trigger any immune response. We found that TaLhcb4.1 interacts with Pt_20 636 , and Pt_20 636 inhibited the function of TaLhcb4.1 involved in wheat resistance to Pt via the ROS pathway. Furthermore, TaLhcb4.1 facilitates Pt_20 636 ‐triggered immune responses in TcLr16 by promoting H 2 O 2 accumulation. Overall, these findings demonstrate the dual role of Pt_20 636 , it subverts TaLhcb4.1‐mediated resistance while eliciting Lr16‐recognized immune signaling, highlighting the complex interplay between fungal virulence and host defense during wheat‐ Pt interactions.